Concomitant exposure to cigarette smoke and coal dust induces lung oxidative stress and decreases serum MUC5AC levels in male rats

• Published in: Biomarkers and genomic medicine Vol. 7; no. 2; pp. 57 - 63
• Main Authors: Kania, Nia, Setiawan, Bambang, Widjajanto, Edi, Nurdiana, Nurdiana, Aris Widodo, M, Chandra Kusuma, H.M.S
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.06.2015
• Subjects: Advanced Basic Science; EGFR signaling; inflammation; Medical Education; oxidative stress; particulate matter; particulate matter; EGFR signaling; inflammation; oxidative stress
• ISSN: 2214-0247; 2214-0255
• DOI: 10.1016/j.bgm.2014.10.001

Abstract This study aimed to investigate whether concomitant exposure to cigarette smoke and coal dust could activate the epidermal growth factor receptor (EGFR) for MUC5AC expression. Thirty-two male Wistar rats were divided into the following groups ( n  = 8 each): control group (C); exposed to cigarette smoke plus coal dust at doses of 6.25 mg/m3 (CS + CD1 ); 12.5 mg/m3 (CS + CD2 ); and 25 mg/m3 (CS + CD3 ). The duration of exposure was 21 days, 1 hour/day. Lung malondialdehyde level was analyzed colorimetrically. Serum EGF and MUC5AC expression were measured by ELISA. Expression of lung EGFR and MUC5AC were measured by a confocal laser scanning microscopy. The level of lung malondialdehyde was higher significantly in all doses of exposure compared with control group ( p  < 0.05). The level of serum EGF was significantly increased in CS + CD2 group compared with control group or CS + CD1 group. The expression of EGFR was not significantly different among all the treatment groups ( p  > 0.05). Serum MUC5AC levels were significantly lower in the two highest doses of coal dust compared with the control group. In conclusion, subchronic combined exposure to cigarette smoke and coal dust induces lung oxidative stress and inflammation and decreases serum MUC5AC level.